The SONG of SHIVA

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had passed them this morning, more curious about Miss Thailand’s dress size, she had been unaware of exactly how much productive research was actually being accomplished in every one of those buzzing cubicles.
    Her head was still spinning in the rarified air of this new technology’s full implications when, just before five that afternoon, she was ushered into another conference room and a second debriefing. Finding an empty chair at the horseshoe-shaped conference table, she sat down just as a large monitor descended from the center of the ceiling and the other participants busily linked individual netbooks to the central server application.
    It had been a productive day. One new antigenic marker had been tentatively identified and another confirmed as actively pathogenic. The expressed protein key-set used to cleave the cellular wall had been documented. Two other equally important expressed protein factors, which could successfully confuse the killer T-cell self-non-self mechanism, had also been located. The exact mechanism for their subterfuge remained a mystery. A special team was formed to investigate. All the result of those elegant Hypothecated Modeling algorithms.
    One of the research team leads, a young Korean microbiologist named Yin Yat Chen, had waited patiently for the others to speak in their assigned order and eventually got her opportunity to present to the group. Switching control of the monitor to her own netbook, she brought up a crisp image of an unassuming segment of the TAI virus’s RNA strand.
    “You know how we were baffled by the precipitous decline in the infection rate beginning about six weeks after the epidemic began? We may have discovered the reason.”
    Not a sound. Nothing but eyes, and all of them fixed on the holographic model, floating as though suspended in dark oil.
    “One entire segment of the strand, sequenced from here to here...” She indicated the specific section using the HM system’s shared cursor, “It appears to be a novel anti-telomerase antibody ― a cleaving protein, that once triggered by some as yet unknown process, then targets the host-cell telomere chains and destroys them on contact.”
    Nora understood immediately why the woman was so excited. Once this anti-telomerase antibody sequence was activated inside an infected cell, that cell would lose all ability to replicate, thereby removing the virus’s only method of propagation.
    The process was particularly beneficial to an infected host. When the body’s specialized scavenger cells ― macrophages ― eventually arrived to remove the now dormant cell, they would also absorb the unique antigens of the trapped virus, producing improved immunologic recognition and antigenic response.
    But why would a virus ever have evolved in such a manner? Nora had run through her silent analysis in the space of a single breath. The microbiologist had taken only one herself.
    “When this sequence expresses,” she continued, “― we have yet to identify the trigger for that expression ― the proteins generated cause the infected cell to enter almost immediate senescence and the cell dies. Why it exists at all is anyone’s guess. It doesn’t make any sense, but there it is.”
    The revelation silenced everyone around the conference table. Why would a virus develop such a mechanism? If borne out by further study, the TAI virus had evolved contrary to the primary biologic imperative.

 
    CHAPTER SEVEN
A Lesson in Desire
    Wonder at the strange dexterity of Fortune’s operations, the facility with which She makes one event the spring and motion of something wholly different, uniting every scattered accident, loose particular and remote action, and interweaves them together to serve Her purpose; so that things which in themselves seem to have no connection or interdependence whatsoever, become in Her hands, the end and beginning of each other.
    Plutarch : The Life of Timoleon
    Lyköan paused in the moonlight at the

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